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PATH STORE > Pulmonary II - Chronic Bronchitis and Emphysema > Flashcards

Pulmonary II - Chronic Bronchitis and Emphysema Flashcards

1
Q

General features of chronic bronchitis - what does a typical patient present like?

A

patient with persistent cough + sputum production for at least 3 mo in at least 2 consecutive years

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2
Q

simple chronic bronchitis

A

productive cough but no evidence of airway obstruction

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3
Q

chronic asthmatic bronchitis

A

intermittent bronchospasm, wheezing - hyper-reactive airways

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4
Q

obstructive chronic bronchitis (heavy smokers)

A

physiologic obstruction +emphysema

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5
Q

Pathogenesis of chronic bronchitis

–what are the two important factors?

A

two factors:

1) chronic irritation by inhaled substances,
2) microbiologic infections

4-10X more common in smokers 

hypersecretion of mucus with mucous plugging

  • –secondary obstruction to air flow
  • –secondary infection
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6
Q

Chronic damage to the epithelium that occurs with chronic bronchitis can lead to …

A

metaplasia

  • –large airways – squamous metaplasia
  • –small airways – goblet cell metaplasia
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7
Q

Increased mucus production seen with chronic bronchitis

  • -associated with …
  • -what accompanying alterations are there?
A

associated with hypertrophy of submucosal glands in
trachea and bronchi

accompanying alterations small airways (2-3 mm)
–marked increase in goblet cells of small airways; mucus plugging of the lumen
–inflammatory infiltration
–fibrosis of the bronchiolar wall
–mucosal secretion is under autonomic (vagal) control;
?hypersecretion caused by neurohormonal pathways (also bronchoconstriction)

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8
Q

Pathogenesis of chronic bronchitis

  • -causes
  • -can coexist with
  • -what is the role of infection
A

smoking and irritants also cause bronchiolitis - early
and relatively mild airflow obstruction

when bronchitis is accompanied by moderate to severe airflow obstruction, coexistent emphysema is the dominant lesion

role of infection is secondary
–not responsible for initiation of chronic bronchitis
–significant in maintaining bronchitis; acute
exacerbations
–cigarette smoke interferes with ciliary action
–also inhibits bronchial and alveolar leukocytes

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9
Q

Gross features of chronic bronchitis

A

hyperemia, swelling, bogginess of mucous
membranes

excessive mucinous to mucopurulent secretions

heavy casts of secretions and pus

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10
Q

Morphology of chronic bronchitis involving the large airways

A

enlargement of mucus-secreting glands of the trachea and bronchi (Reid Index)

  • –ratio of the thickness of mucosal glands to the thickness of wall between the epithelium and the cartilage; normally < 0.4
  • –increased in proportion to severity and duration of the disease

squamous metaplasia and dysplasia of large airways

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11
Q

Morphology of chronic bronchitis involving the small airways

A

marked narrowing of bronchioles - goblet cell metaplasia,mucous plugging, inflammation, and fibrosis

most severe cases - bronchiolitis obliterans

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17
Q

General feature of emphysema

  • -what is it?
  • -how does this happen?
  • -associations?
  • -clinical ventilatory defects??
A

abnormal permanent enlargement of the airspaces distal to the terminal bronchiole

  • -enlargement due to destruction of walls without obvious fibrosis (overinflation)
    • –particularly destroying elastin
  • -involves expansion of terminal bronchiole and acini, including alveolar ducts

–cleat-cut association with heavy cigarette
smoking

–clinical ventilatory deficits early, but not symptomatic until late

18
Q

What are the two main issues with emphysema?

A
  1. Decreased FEV1
    —collapse/obstruction of terminal airways on
    expiration decreased FEV1 “pink puffers”
    —can open airways OK, so well oxygenated
    —symptoms occur only after extensive destruction of lung
    tissue
    —barrel-chested with faint breath sounds
  2. Destruction of terminal airways;formation of bullae
    - –Thin-walled coalescing of airspaces; not fibrotic
19
Q

What are the different types of emphysema?

A
  1. Centriacinar (centilobular) emphysema
  2. Panacinar (panlobular) emphysema
  3. Paraseptal (distal acinar) emphysema
20
Q

Centriacinar (centilobular) emphysema

A

central or proximal parts of the acini formed by the respiratory bronchioles
–both emphysematous and normal airspaces exist more common and severe in upper lobes (apical
segments)
–inflammation in septa with deposit of black pigment
–associated with smoking and chronic bronchitis, coal
worker’s pneumoconiosis

21
Q

Panacinar (panlobular) emphysema

A

acini are uniformly enlarged including respiratory bronchiole and terminal blind alveoli
–prefix pan- refers to entire acinus, not entire lung
–occurs more commonly in lower zone and anterior
margins of lung
–most severe at bases
–associated with alpha1-antitrypsin deficiency

22
Q

Paraseptal (distal acinar) emphysema

A

proximal portion of acinus is normal; distal portion dominantly involved

  • -more striking adjacent to the pleura, along tissue septa, and margins of lobules
  • -adjacent to areas of fibrosis, scarring, or atelectasis
  • -more severe in upper half of lungs
  • -multiple, continuous, enlarged airspaces to > 2.0 cm
  • -?associated with spontaneous pneumothorax in young
23
Q

Main theory in the pathogenesis of emphysema

  • -what mechanism if responsible?
  • -what does this mean in terms of the wall destruction?
  • -what is the result of destruction?
A

protease-antiprotease mechanism
–alveolar wall destruction results from imbalance of
proteases (elastase) and anti-proteases
–increased protease activity leads to break-down of elastic components in the alveoli and airways
–results in loss of elastic recoil
–decreased spontaneous release of air from alveoli on expiration
–terminal airways collapse under positive expiratory pressures due to decreased structural components

24
Q

Alpha-1 anti-tryspsin deficiency and emphysema relation

  • -what kind of activity?
  • -why is alpha 1 AT important?
  • -where does the principle elastase come from?
A

This is due to decreased anti-elastase activity

  • -homozygous patients with alpha1-antitrypsin develop emphysema
    • –alpha 1-AT major inhibitor of proteases including elastase
  • -principle elastase from neutrophils
    • –neutrophils normally sequestered in lung (more in lower zones)
    • –leads to elastase-mediated destruction of elastin

–The most important therapeutic intervention is cessation of smoking

25
Q

Smoking and emphysema relation

  • -what kind of activity?
  • -what does smoking do to balance of cells?
  • -what is nicotine’s role?
A

Increased elastase activity

  • -smokers have greater numbers of neutrophils and macrophages in alveoli secondary to release of IL-8 from activated macrophages
  • -nicotine is chemotactic for neutrophils and cigarette smoke activates the alternative complement pathway
  • -smoking stimulates elastase from neutrophils and macrophages (macrophage elastase is NOT inhibited by alpha 1-AT)
  • -oxidants in cigarette smoke and oxygen free radicals inhibit alpha 1-AT activity
26
Q

Macroscopic morphology of emphysema

–what is the difference between panacinar and centrilobular?

A

panacinar emphysema - voluminous lungs

centrilobular emphysema - not as voluminous; upper
2/3 affected

large apical blebs or bullae characteristic of irregular emphysema secondary to scarring

27
Q

Microscopic morphology of emphysema

A

abnormal fenestrations and destruction of septal walls

fusion of alveoli to form blebs or bullae

respiratory bronchioles and vasculature deformed and compressed by distortion of airspaces

28
Q

Clinical features of emphysema

A

clinical manifestations do not appear until at least 1/3 of functioning parenchyma is incapacitated

dyspnea progresses; may see cough or wheezing

weight loss may be severe

slowing of forced expiration!!!!!!

barrel-chested with prolonged expiratory effort

29
Q

Senile emphysema

A

age-related alterations of the internal geometry of the lung (larger alveolar ducts and smaller alveoli)

30
Q

Obstructive oveinflation

A

trapping of air

31
Q

Bullous emphysema

A

(>1 cm in distended state)

often apical, associated with scarring

may give rise to pneumothorax

32
Q

Interstitial emphysema

A

entrance of air into connective tissue stroma, mediastinum, or subcutaneous tissue

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